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Medicina (Kaunas, Lithuania) 2008Coma is the disorder of consciousness because of the damage to diffused bilateral cerebral hemisphere cortex or reticular activating system. Coma can be caused by... (Review)
Review
Coma is the disorder of consciousness because of the damage to diffused bilateral cerebral hemisphere cortex or reticular activating system. Coma can be caused by neurogenic (head brain injury), metabolic (endogenic), and toxic (exogenic) factors. To determine the cause of metabolic and toxic coma, laboratory tests are performed; in case of neurogenic coma, the neurologic examination is essential, when five systems are evaluated: the level of consciousness (according to Glasgow Coma Scale or Full Outline of Unresponsiveness Scale), photoreaction of pupils and ophthalmoscopic examination, oculomotoric, motoric, and cardiopulmonary systems. For the treatment of coma, adequate oxygenation and correction of blood circulation disorders are important. The treatment of metabolic coma is guided by special schemes; antidotes often are needed in the treatment of toxic coma, and surgery helps if traumatic brain injury is present. The prognosis and outcomes of the comatose patient depend on the age and comorbid diseases of the patient, the underlying cause of coma, timely medical help and its quality, and intensive treatment and care of the patient in coma.
Topics: Aged; Brain Death; Coma; Confusion; Critical Care; Diagnosis, Differential; Electroencephalography; Glasgow Coma Scale; Humans; Lethargy; Magnetic Resonance Imaging; Prognosis; Sepsis; Stupor; Time Factors
PubMed: 19001840
DOI: No ID Found -
Medicina 2017Hypothyroidism is a frequently diagnosed and simply treated disease. If not recognised, however, in time it may develop into the most severe manifestation of... (Review)
Review
Hypothyroidism is a frequently diagnosed and simply treated disease. If not recognised, however, in time it may develop into the most severe manifestation of hypothyroidism known as myxedema coma. The term "myxedema coma" is generally seen as misleading since most patients do not initially present in a coma. The typical progression is lethargy evolving into stupor and, eventually, into coma with respiratory failure and hypothermia. It mainly affects elderly women, often occurring in winter and is relatively rare. It can be considered a form of decompensated hypothyroidism often triggered by a variety of non-thyroid conditions or diseases provoking an extremely severe condition of multiple system failure with lethal consequences unless an early diagnosis is made and an aggressive treatment is administered.
Topics: Coma; Disease Progression; Humans; Hypothyroidism; Myxedema
PubMed: 28825577
DOI: No ID Found -
Toxins Feb 2021For thousands of years, has been utilized as a medicine and for recreational and spiritual purposes. Phytocannabinoids are a family of compounds that are found in the... (Review)
Review
For thousands of years, has been utilized as a medicine and for recreational and spiritual purposes. Phytocannabinoids are a family of compounds that are found in the cannabis plant, which is known for its psychotogenic and euphoric effects; the main psychotropic constituent of cannabis is Δ9-tetrahydrocannabinol (Δ9-THC). The pharmacological effects of cannabinoids are a result of interactions between those compounds and cannabinoid receptors, CB1 and CB2, located in many parts of the human body. Cannabis is used as a therapeutic agent for treating pain and emesis. Some cannabinoids are clinically applied for treating chronic pain, particularly cancer and multiple sclerosis-associated pain, for appetite stimulation and anti-emesis in HIV/AIDS and cancer patients, and for spasticity treatment in multiple sclerosis and epilepsy patients. Medical cannabis varies from recreational cannabis in the chemical content of THC and cannabidiol (CBD), modes of administration, and safety. Despite the therapeutic effects of cannabis, exposure to high concentrations of THC, the main compound that is responsible for most of the intoxicating effects experienced by users, could lead to psychological events and adverse effects that affect almost all body systems, such as neurological (dizziness, drowsiness, seizures, coma, and others), ophthalmological (mydriasis and conjunctival hyperemia), cardiovascular (tachycardia and arterial hypertension), and gastrointestinal (nausea, vomiting, and thirst), mainly associated with recreational use. Cannabis toxicity in children is more concerning and can cause serious adverse effects such as acute neurological symptoms (stupor), lethargy, seizures, and even coma. More countries are legalizing the commercial production and sale of cannabis for medicinal use, and some for recreational use as well. Liberalization of cannabis laws has led to increased incidence of toxicity, hyperemesis syndrome, lung disease cardiovascular disease, reduced fertility, tolerance, and dependence with chronic prolonged use. This review focuses on the potential therapeutic effects of cannabis and cannabinoids, as well as the acute and chronic toxic effects of cannabis use on various body systems.
Topics: Animals; Cannabinoids; Cannabis; Humans; Marijuana Abuse; Medical Marijuana; Nervous System; Neurotoxicity Syndromes; Plants, Toxic; Receptors, Cannabinoid; Signal Transduction
PubMed: 33562446
DOI: 10.3390/toxins13020117 -
Gastroenterology Report May 2017Hepatic encephalopathy (HE) is a reversible syndrome of impaired brain function occurring in patients with advanced liver diseases. The precise pathophysiology of HE is...
Hepatic encephalopathy (HE) is a reversible syndrome of impaired brain function occurring in patients with advanced liver diseases. The precise pathophysiology of HE is still under discussion; the leading hypothesis focus on the role of neurotoxins, impaired neurotransmission due to metabolic changes in liver failure, changes in brain energy metabolism, systemic inflammatory response and alterations of the blood brain barrier. HE produces a wide spectrum of nonspecific neurological and psychiatric manifestations. Minimal HE is diagnosed by abnormal psychometric tests. Clinically overt HE includes personality changes, alterations in consciousness progressive disorientation in time and space, somnolence, stupor and, finally, coma. Except for clinical studies, no specific tests are required for diagnosis. HE is classified according to the underlying disease, the severity of manifestations, its time course and the existence of precipitating factors. Treatment of overt HE includes supportive therapies, treatment of precipitating factors, lactulose and/or rifaximin. Routine treatment for minimal HE is only recommended for selected patients.
PubMed: 28533911
DOI: 10.1093/gastro/gox013 -
Geriatrie Et Psychologie... Mar 2019Non-convulsive status epilepticus (NCSE) is common in the elderly. It most often corresponds to prolonged focal seizures with impaired contact ("complex partial status... (Review)
Review
Non-convulsive status epilepticus (NCSE) is common in the elderly. It most often corresponds to prolonged focal seizures with impaired contact ("complex partial status epilepticus"). A form of de novo absence status epilepticus, much rarer, can also meet. The identified risk factors for NCSE onset are: a precession by a generalized tonic-clonic seizure, a known history of epilepsy, female gender, and known brain injury (especially a stroke sequelae). The presence of one of these risk factors combined with a confusional picture of unknown origin should lead us to think of the diagnosis of NCSE. As the clinic is often not very suggestive (stupor, confusion, even coma), the diagnosis will be based on the EEG with criteria now accepted (so-called Salzburg EEG criteria). The treatment is based first on the injection of benzodiazepines and in the second line on intravenous or oral or gastric tube administration of antiepileptic drugs. It is not recommended to resort to an intubation-ventilation (except need out treatment of the state of evil: respiratory distress, multi-organ failure…). The prognosis is generally poor with about 30% mortality.
Topics: Aged; Aged, 80 and over; Anticonvulsants; Electroencephalography; Female; Humans; Male; Risk Factors; Status Epilepticus
PubMed: 30916648
DOI: 10.1684/pnv.2019.0782 -
Nature Sep 2022Infections induce a set of pleiotropic responses in animals, including anorexia, adipsia, lethargy and changes in temperature, collectively termed sickness behaviours....
Infections induce a set of pleiotropic responses in animals, including anorexia, adipsia, lethargy and changes in temperature, collectively termed sickness behaviours. Although these responses have been shown to be adaptive, the underlying neural mechanisms have not been elucidated. Here we use of a set of unbiased methodologies to show that a specific subpopulation of neurons in the brainstem can control the diverse responses to a bacterial endotoxin (lipopolysaccharide (LPS)) that potently induces sickness behaviour. Whole-brain activity mapping revealed that subsets of neurons in the nucleus of the solitary tract (NTS) and the area postrema (AP) acutely express FOS after LPS treatment, and we found that subsequent reactivation of these specific neurons in FOS (also known as TRAP2) mice replicates the behavioural and thermal component of sickness. In addition, inhibition of LPS-activated neurons diminished all of the behavioural responses to LPS. Single-nucleus RNA sequencing of the NTS-AP was used to identify LPS-activated neural populations, and we found that activation of ADCYAP1 neurons in the NTS-AP fully recapitulates the responses elicited by LPS. Furthermore, inhibition of these neurons significantly diminished the anorexia, adipsia and locomotor cessation seen after LPS injection. Together these studies map the pleiotropic effects of LPS to a neural population that is both necessary and sufficient for canonical elements of the sickness response, thus establishing a critical link between the brain and the response to infection.
Topics: Animals; Anorexia; Area Postrema; Brain Stem; Illness Behavior; Lethargy; Lipopolysaccharides; Mice; Neurons; Pituitary Adenylate Cyclase-Activating Polypeptide; Proto-Oncogene Proteins c-fos; Solitary Nucleus
PubMed: 36071158
DOI: 10.1038/s41586-022-05161-7 -
BMJ Case Reports Jan 2019A 60-year-old man with cerebral palsy and epilepsy was admitted with acute lethargy and deterioration in coordination. He was noted to be hypothermic at 35°C on...
A 60-year-old man with cerebral palsy and epilepsy was admitted with acute lethargy and deterioration in coordination. He was noted to be hypothermic at 35°C on admission. Routine work-up revealed toxic levels of phenytoin. No cause of hypothermia could be identified but as his phenytoin levels normalised, his body temperature also improved. There are three other reported cases of phenytoin- induced hypothermia in the literature. Could this be a rare cause of hypothermia?
Topics: Aftercare; Ataxia; Cytochrome P-450 CYP1A2 Inducers; Diagnosis, Differential; Humans; Hypothermia; Lethargy; Male; Middle Aged; Phenytoin; Treatment Outcome
PubMed: 30674493
DOI: 10.1136/bcr-2018-227443 -
British Medical Journal Jun 1948
Topics: Anesthetics; Convulsive Therapy; Electricity; Electroconvulsive Therapy; Humans; Stupor
PubMed: 18865967
DOI: 10.1136/bmj.1.4562.1156